Respiratory muscle fatigue during cardiogenic shock.
The effect of cardiogenic shock (tamponade) on respiratory muscles performance was studied in 13 dogs breathing spontaneously. These 13 dogs were compared with 7 dogs artificially ventilated and paralyzed. Cardiac output amounted in both groups to 25-35% of the control value and was maintained constant. None of the dogs were hypoxic. All the spontaneously breathing dogs died on the average 140 +/- 15 min after the onset of cardiogenic shock, whereas the seven dogs artificially ventilated were all alive after 3 h and then killed. Death in the spontaneously breathing dogs was secondary to respiratory failure. Transdiaphragmatic pressure increased during the 1st h by 152 +/- 25% of control and then decreased by 286 +/- 18% in relation to the peak value before the death of the animals. No major changes in the mechanical properties of the respiratory system occurred. The decrease in transdiaphragmatic pressure occurred despite a marked increase per breath in the amplitude of the integrated electrical activity of the diaphragm and of the phrenic nerve. It is concluded that the ventilatory failure of cardiogenic shock is due to an impairment of the contractile process of the respiratory muscles. Artificial ventilation avoids respiratory failure and prolongs survival, which may bear important therapeutic implications.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002302:Cardiac Output; D003964:Diaphragm / Q000503:physiopathology*; D004285:Dogs; D005221:Fatigue / Q000503:physiopathology*; D009119:Muscle Contraction; D010100:Oxygen / Q000097:blood; D010313:Partial Pressure; D010791:Phrenic Nerve / Q000503:physiopathology; D012121:Respiration, Artificial; D012770:Shock, Cardiogenic / Q000503:physiopathology*; D013997:Time Factors
D002245:Carbon Dioxide; D010100:Oxygen